@article{BuchmannHellwegRietscheletal.2013,
  author    = {Buchmann, Arlette F. and Hellweg, Rainer and Rietschel, Marcella and Treutlein, Jens and Witt, Stephanie H. and Zimmermann, Ulrich S. and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Laucht, Manfred and Deuschle, Michael},
  title     = {BDNF Val 66 Met and 5-HTTLPR genotype moderate the impact of early psychosocial adversity on plasma brain-derived neurotrophic factor and depressive symptoms - a prospective study},
  series = {European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology},
  volume    = {23},
  journal   = {European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology},
  number    = {8},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0924-977X},
  doi       = {10.1016/j.euroneuro.2012.09.003},
  pages     = {902 -- 909},
  year      = {2013},
  abstract  = {Recent studies have emphasized an important role for neurotrophins, such as brain-derived neurotrophic factor (BDNF), in regulating the plasticity of neural circuits involved in the pathophysiology of stress-related diseases. The aim of the present study was to examine the interplay of the BDNF Val(66)Met and the serotonin transporter promoter (5-HTTLPR) polymorphisms in moderating the impact of early-life adversity on BDNF plasma concentration and depressive symptoms. Participants were taken from an epidemiological cohort study following the long-term outcome of early risk factors from birth into young adulthood. In 259 individuals (119 males, 140 females), genotyped for the BDNF Val(66)Met and the 5-HTTLPR polymorphisms, plasma BDNF was assessed at the age of 19 years. In addition, participants completed the Beck Depression Inventory (BDI). Early adversity was determined according to a family adversity index assessed at 3 months of age. Results indicated that individuals homozygous for both the BDNF Val and the 5-HTTLPR L allele showed significantly reduced BDNF levels following exposure to high adversity. In contrast, BDNF levels appeared to be unaffected by early psychosocial adversity in carriers of the BDNF Met or the 5-HTTLPR S allele. While the former group appeared to be most susceptible to depressive symptoms, the impact of early adversity was less pronounced in the latter group. This is the first preliminary evidence indicating that early-life adverse experiences may have lasting sequelae for plasma BDNF levels in humans, highlighting that the susceptibility to this effect is moderated by BDNF Val(66)Met and 5-HTTLPR genotype.},
  language  = {en}
}
@article{KalliesRappFydrichetal.2018,
  author    = {Kallies, Gunnar and Rapp, Michael A. and Fydrich, Thomas and Fehm, Lydia and Tschorn, Mira and Teran, Christina and Schwefel, Melanie and Pietrek, Anou F. and Henze, Romy and Hellweg, Rainer and Str{\"o}hle, Andreas and Heinzel, Stephan and Heissel, Andreas},
  title     = {Serum brain-derived neurotrophic factor (BDNF) at rest and after acute aerobic exercise in major depressive disorder},
  series = {Psychoneuroendocrinology},
  volume    = {102},
  journal   = {Psychoneuroendocrinology},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0306-4530},
  doi       = {10.1016/j.psyneuen.2018.12.015},
  pages     = {212 -- 215},
  year      = {2018},
  abstract  = {Physiological mechanisms of an anti-depressive effect of physical exercise in major depressive disorder (MDD) seem to involve alterations in brain-derived neurotrophic factor (BDNF) level. However, previous studies which investigated this effect in a single bout of exercise, did not control for confounding peripheral factors that contribute to BDNF-alterations. Therefore, the underlying cause of exercise-induced BDNF-changes remains unclear. The current study aims to investigate serum BDNF (sBDNF)-changes due to a single-bout of graded aerobic exercise in a group of 30 outpatients with MDD, suggesting a more precise analysis method by taking plasma volume shift and number of platelets into account. Results show that exercise-induced increases in sBDNF remain significant (p<.001) when adjusting for plasma volume shift and controlling for number of platelets. The interaction of sBDNF change and number of platelets was also significant (p=.001) indicating larger sBDNF-increase in participants with smaller number of platelets. Thus, findings of this study suggest an involvement of peripheral as well as additional possibly brain-derived mechanisms explaining exercise-related BDNF release in MDD. For future studies in the field of exercise-related BDNF research, the importance of controlling for peripheral parameters is emphasized.},
  language  = {en}
}
@misc{KuhlmannTschornAroltetal.2017,
  author    = {Kuhlmann, Stella L. and Tschorn, Mira and Arolt, Volker and Beer, Katja and Brandt, Julia and Grosse, Laura and Haverkamp, Wilhelm and Mueller-Nordhorn, Jacqueline and Rieckmann, Nina and Waltenberger, Johannes and Warnke, Katharina and Hellweg, Rainer and Stroehle, Andreas},
  title     = {Serum brain-derived neurotrophic factor and depressive symptoms in coronary heart disease patients: Role of cognitive functions Reply},
  series = {Psychoneuroendocrinology},
  volume    = {79},
  journal   = {Psychoneuroendocrinology},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0306-4530},
  doi       = {10.1016/j.psyneuen.2017.02.010},
  pages     = {175 -- 176},
  year      = {2017},
  language  = {en}
}
@article{KuhlmannTschornAroltetal.2017,
  author    = {Kuhlmann, Stella and Tschorn, Mira and Arolt, Volker and Beer, Katja and Brandt, Julia and Grosse, Laura and Haverkamp, Wilhelm and M{\"u}ller-Nordhorn, Jacqueline and Rieckmann, Nina and Waltenberger, Johannes and Warnke, Katharina and Hellweg, Rainer and Str{\"o}hle, Andreas},
  title     = {Serum brain-derived neurotrophic factor and stability of depressive symptoms in coronary heart disease patients},
  series = {Psychoneuroendocrinology : an international journal ; the official journal of the International Society of Psychoneuroendocrinology},
  volume    = {77},
  journal   = {Psychoneuroendocrinology : an international journal ; the official journal of the International Society of Psychoneuroendocrinology},
  publisher = {Elsevier Science},
  address   = {Oxford},
  issn      = {0306-4530},
  doi       = {10.1016/j.psyneuen.2016.12.015},
  pages     = {196 -- 202},
  year      = {2017},
  abstract  = {Objective: Brain-derived neurotrophic factor (BDNF) supports neurogenesis, angiogenesis, and promotes the survival of various cell types in the brain and the coronary system. Moreover, BDNF is associated with both coronary heart disease (CHD) and depression. The current study aims to investigate whether serum BDNF levels are associated with the course of depressive symptoms in CHD patients. Methods: At baseline, N = 225 CHD patients were enrolled while hospitalized. Of these, N = 190 (84\%) could be followed up 6 months later. Depressive symptoms were assessed both at baseline and at the 6-months follow-up using the Patient Health Questionnaire (PHQ-9). Serum BDNF concentrations were measured using fluorometric Enzyme-linked immunosorbent assays (ELISA). Results: Logistic regression models showed that lower BDNF levels were associated with persistent depressive symptoms, even after adjustment for age, sex, smoking and potential medical confounders. The incidence of depressive symptoms was not related to lower BDNF levels. However, somatic comorbidity (as measured by the Charlson Comorbidity Index) was significantly associated with the incidence of depressive symptoms. Conclusions: Our findings suggest a role of BDNF in the link between CHD and depressive symptoms. Particularly, low serum BDNF levels could be considered as a valuable biomarker for the persistence of depressive symptoms among depressed CHD patients.},
  language  = {en}
}
@article{StroehleSchmidtSchultzetal.2015,
  author    = {Stroehle, Andreas and Schmidt, Dietlinde K. and Schultz, Florian and Fricke, Nina and Staden, Theresa and Hellweg, Rainer and Priller, Josef and Rapp, Michael A. and Rieckmann, Nina},
  title     = {Drug and Exercise Treatment of Alzheimer Disease and Mild Cognitive Impairment: A Systematic Review and Meta-Analysis of Effects on Cognition in Randomized Controlled Trials},
  series = {The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry},
  volume    = {23},
  journal   = {The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry},
  number    = {12},
  publisher = {Elsevier},
  address   = {New York},
  issn      = {1064-7481},
  doi       = {10.1016/j.jagp.2015.07.007},
  pages     = {1234 -- 1249},
  year      = {2015},
  abstract  = {Objective: Demographic changes are increasing the pressure to improve therapeutic strategies against cognitive decline in Alzheimer disease (AD) and mild cognitive impairment (MCI). Besides drug treatment, physical activity seems to be a promising intervention target as epidemiological and clinical studies suggest beneficial effects of exercise training on cognition. Using comparable inclusion and exclusion criteria, we analyzed the efficacy of drug therapy (cholinesterase inhibitors, memantine, and Ginkgo biloba) and exercise interventions for improving cognition in AD and MCI populations. Methods: We searched The Cochrane Library, EBSCO, OVID, Web of Science, and U.S Food and Drug Administration data from inception through October 30, 2013. Randomized controlled trials in which at least one treatment arm consisted of an exercise or a pharmacological intervention for AD or MCI patients, and which had either a non-exposed control condition or a control condition that received another intervention. Treatment discontinuation rates and Standardized Mean Change score using Raw score standardization (SMCR) of cognitive performance were calculated. Results: Discontinuation rates varied substantially and ranged between 0\% and 49\% with a median of 18\%. Significantly increased discontinuation rates were found for galantamine and rivastigmine as compared to placebo in AD studies. Drug treatments resulted in a small pooled effect on cognition (SMCR: 0.23, 95\% CI: 0.20 to 0.25) in AD studies (N = 45, 18,434 patients) and no effect in any of the MCI studies (N = 5, 3,693 patients; SMCR: 0.03, 95\% CI: 0.00 to 0.005). Exercise interventions had a moderate to strong pooled effect size (SMCR: 0.83, 95\% CI: 0.59 to 1.07) in AD studies (N = 4, 119 patients), and a small effect size (SMCR: 0.20, 95\% CI: 0.11 to 0.28) in MCI (N = 6, 443 patients). Conclusions: Drug treatments have a small but significant impact on cognitive functioning in AD and exercise has the potential to improve cognition in AD and MCI. Head-to-head trials with sufficient statistical power are necessary to directly compare efficacy, safety, and acceptability. Combining these two approaches might further increase the efficacy of each individual intervention. Identifier: PROSPERO (2013:CRD42013003910).},
  language  = {en}
}
@misc{TschornKuhlmannRieckmannetal.2020,
  author    = {Tschorn, Mira and Kuhlmann, Stella Linnea and Rieckmann, Nina and Beer, Katja and Grosse, Laura and Arolt, Volker and Waltenberger, Johannes and Haverkamp, Wilhelm and M{\"u}ller-Nordhorn, Jacqueline and Hellweg, Rainer and Str{\"o}hle, Andreas},
  title     = {Brain-derived neurotrophic factor, depressive symptoms and somatic comorbidity in patients with coronary heart disease},
  series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  journal   = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  number    = {1},
  issn      = {1866-8364},
  doi       = {10.25932/publishup-55731},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-557315},
  pages     = {11},
  year      = {2020},
  abstract  = {Objective: Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF). Methods: The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment. Results: Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS. Conclusion: Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.},
  language  = {en}
}
@article{TschornKuhlmannRieckmannetal.2020,
  author    = {Tschorn, Mira and Kuhlmann, Stella Linnea and Rieckmann, Nina and Beer, Katja and Grosse, Laura and Arolt, Volker and Waltenberger, Johannes and Haverkamp, Wilhelm and M{\"u}ller-Nordhorn, Jacqueline and Hellweg, Rainer and Str{\"o}hle, Andreas},
  title     = {Brain-derived neurotrophic factor, depressive symptoms and somatic comorbidity in patients with coronary heart disease},
  series = {Acta Neuropsychiatrica},
  volume    = {33},
  journal   = {Acta Neuropsychiatrica},
  number    = {1},
  publisher = {Cambridge Univ. Press},
  address   = {Cambridge},
  issn      = {1601-5215},
  doi       = {10.1017/neu.2020.31},
  pages     = {22 -- 30},
  year      = {2020},
  abstract  = {Objective: Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF). Methods: The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment. Results: Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS. Conclusion: Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.},
  language  = {en}
}